Parainflammation, Chronic Inflammation and Age-Related Macular Degeneration
Open accessAbstract
Inflammation is an adaptive response of the immune system to noxious insults to maintain homeostasis and restore functionality. The retina is considered an immune-privileged tissue as a result of its unique anatomic and physiologic properties. During aging, the retina suffers from a low-grade chronic oxidative insult, which sustains for decades and increases in level with advancing age. As a result, the retinal innate-immune system, particularly microglia and the complement system, undergoes low levels of activation (parainflammation). In many cases, this parainflammatory response can maintain homeostasis in the healthy aging eye. However, in patients with age-related macular degeneration, this parainflammatory response becomes dysregulated and contributes to macular damage. Factors contributing to the dysregulation of age-related retinal parainflammation include genetic predisposition, environmental risk factors, and old age. Dysregulated parainflammation (chronic inflammation) in age-related macular degeneration damages the blood retina barrier, resulting in the breach of retinal-immune privilege, leading to the development of retinal lesions. This review discusses the basic principles of retinal innate-immune responses to endogenous chronic insults in normal aging and in age-related macular degeneration and explores the difference between beneficial parainflammation and the detrimental chronic inflammation in the context of age-related macular degeneration.
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Danger signals in the retina may result in mild activation of the innate immune system, termed para-inflammation.
“While the immune tolerance mechanism tries to counterbalance inflammation, danger signals in the retina may still result in mild activation of the innate immune system, in a process recently termed para-inflammation [27][28][29].”
From Risk mitigation of immunogenicity: a key to personalized retinal gene therapy (2021) · cites this paper as [29]
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Risk mitigation of immunogenicity: a key to personalized retinal gene therapy
Varin, J., Morival, C., Maillard, N., Adjali, O., & Cronin, T. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222312818 · Cited by 19 · see citing works
Adamus, G. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2021.672444 · Cited by 16 · see citing works
Gyenes, A., István, L., Benyó, F., Papp, A., Resch, M., Sándor, N., Józsi, M., Nagy, Z. Z., Kovács, I., & Kiss, S. (2023) · BMC Ophthalmology · doi:10.1186/s12886-022-02761-9 · Cited by 9 · see citing works
- Authors
- Chen, M., & Xu, H.
- Affiliations
- Queen's University Belfast (GB)
- Corresponding author
- Xu, Heping
- ORCID
- Venue
- Journal of Leukocyte Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2015-08-20
- Volume
- 98
- Issue
- 5
- Pages
- 713-725
- ISSN
- 0741-5400 (ISSN-L)
- 1938-3673
- PMC
- PMC4733662
- OpenAlex
- W2209285888
- Cited by
- 381
- References
- 189
- Citations by year
- 2026: 29 · 2025: 39 · 2024: 49 · 2023: 48 · 2022: 44 · 2021: 50 · 2020: 39 · 2019: 25 · 2018: 24 · 2017: 20 · 2016: 12 · 2015: 2
- FWCI
- 3.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Leukocyte Biology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Funders
- Fight for Sight (1361/1362, 1425/1426)
- Dunhill Medical Trust (R188/0211)
- National Eye Research Center (061)
- Topics
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Retinal Imaging and Analysis
- Keywords
- age-related macular degeneration, parainflammation, chronic inflammation, microglia, complement system, blood-retinal barrier, oxidative stress, genetic susceptibility, environmental risk factors
- MeSH terms
- Aging, Animals, Chronic Disease, Humans, Immunity, Innate, Inflammation, Macular Degeneration, Microglia, Genetic Predisposition to Disease
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